Monthly Archive January 2019

Atrial fibrillation classification

Atrial fibrillation classification

Isolated (ie, idiopathic) atrial fibrillation (AF), which occurs in patients younger than 60 years of age, is very common. Although the prognosis is good and the risk of systemic embolism is low (approximately 1.3% over a 15-year period), idiopathic AF can cause very serious symptoms and patient anxiety. Like a “secondary” OP, an isolated OP can be paroxysmal or persistent.

Paroxysmal isolated atrial fibrillation

Only one or several very rare episodes of arrhythmia are possible, but in some cases atrial fibrillation (AF) often recurs, sometimes several times a day.
Paroxysms can last for many hours or end in a few seconds. Over time, some patients (but not all) of AF become persistent.

Studies show that an episode of atrial fibrillation (AF) can lead to changes in the electrical properties of the atria that help to maintain arrhythmias — this process is referred to as “electrical remodeling.”

Often, patients have very serious symptoms. In other cases, including frequent relapses occurring with a high frequency of ventricular contractions, arrhythmia may be asymptomatic or accompanied only by the sensation of arrhythmia, without any discomfort due to high heart rate.

Only some patients can name the factors immediately preceding the arrhythmia and, possibly, provoking it (such as physical exertion, vomiting, alcohol intake or fatigue). One of the forms of paroxysmal idiopathic AF is caused by an increase in the tone of the vagus nerve: an arrhythmia always begins during rest or sleep.

Causes of atrial fibrillation and their prognosis

Causes of atrial fibrillation and their prognosis

The most common causes are damage to or impairment of the function of the heart muscle as a result of myocardial infarction, hypertension or cardiomyopathy, as well as valvular heart disease, hyperthyroidism, and SSS. In many cases, AF is idiopathic, i.e. without any obvious reason.

IHD (i.e., stenosing atherosclerosis of the coronary arteries) is not in itself a cause of atrial fibrillation (AF). However, arrhythmia often complicates myocardial infarction in both acute and long-term periods and serves as an indicator of extensive myocardial damage.

Many of the listed causes of atrial fibrillation (AF) can be identified or excluded by clinical examination, ECG and echocardiography. To exclude hyperthyroidism, it is necessary to determine the level of thyroxine and thyroid-stimulating hormone in the serum. If an SSS is suspected, outpatient ECG monitoring may be required.

Prevalence of Atrial Fibrillation (AF)

The prevalence of atrial fibrillation (AF) increases with age. In the UK, when examining male civil servants, FP was found at 0.16, 0.37 and 1.13% of people aged 40–49, 50–59 and 60–64 years, respectively. Among patients monitored by British general practitioners, arrhythmia was detected in 3.7% of patients over 65 years of age.

According to the Framingham study, it was found that 7.8% of men aged 65-74 years suffer from atrial fibrillation (AF). The prevalence of arrhythmias among men aged 75-84 increases to 11.7%. It is estimated that the probability of occurrence of AF in a person’s life is 26%.

Even among those who do not have heart failure and do not tolerate myocardial infarction, this risk is about 15%. In men, arrhythmia occurs 1.5 times more often than in women.

Atrial fibrillation (AF) prognosis

The main factor determining the prognosis is the presence or absence of organic heart disease. For example, with MI, the prognosis is unfavorable, since AF is usually the result of extensive myocardial damage. Many studies have shown that with idiopathic AF, the prognosis is favorable.

AV conduction

AV conduction

AV conduction increases with an increase in sympathetic activity and is suppressed with an increase in the tone of the vagus nerve. Usually, during periods of patient activity, the frequency of ventricular contractions is high (up to 200 beats / min), while at rest or during sleep it decreases.

Absolutely irregular ventricular rhythm indicates the presence of AF, no matter how small or large the frequency of ventricular contractions.

Intraventricular conduction. Ventricular complexes with FP have a normal duration, except for cases of blockade of the bundle of the His, WPW syndrome or aberrant intraventricular conduction, i.e. frequency-dependent blockade of the bundle branch block. Aberrant intraventricular conduction.

Aberrant conduction is the result of different lengths of the recovery period (i.e. the exit period from the refractoriness state) in the two legs of the His bundle. An early atrial impulse can reach the ventricles at a time when one of the legs of the bundle of His is still refractory to activation after the previous cardiac cycle, while the other is already capable of conduction.

As a result, the ventricular complex will have a configuration characteristic of the blockade of the corresponding bundle of the His. Since the right leg usually has a longer refractory period, aberrant conduction usually leads to blockade of PNPG. The duration of the refractory period of the feet of the bundle of His depends on the duration of the previous cardiac cycle. Therefore, an aberration of conducting is more likely to occur when a short cycle follows a long one (the “Ashman phenomenon”). Sometimes a series of aberrant complexes can be mistakenly interpreted as paroxysmal ventricular tachycardia.

However, even if the frequency of ventricular contractions is very high, it is possible to reveal a distinct irregularity of the cardiac cycle; In addition, the question is legitimate: why during AF, there must be “jogging” of another arrhythmia?

The occurrence of atrial fibrillation. AF is usually initiated by atrial extrasystole. Sometimes TP or ABPT is transformed into fibrillation.

Atrial fibrillation

Atrial fibrillation

Atrial fibrillation (AF) is the most common arrhythmia. Indeed, due to the increase in life expectancy in the population as a whole, and among patients with heart disease, its prevalence is constantly increasing.

It is important to know the various causes and clinical manifestations of arrhythmia and to understand that the tactics of treatment should be individualized depending on the etiology associated with the risk of arrhythmia and the symptoms present.

When atrial fibrillation (AF), the atria are activated with a frequency of 350 to 600 imp./min. Arrhythmia is caused by the existence of numerous excitation waves circulating in random directions within the atrial myocardium. A very high frequency of electrical activity leads to the loss of effective mechanical atrial systole.

1) Atrial activity in atrial fibrillation. High-frequency and chaotic electrical activity of the atria during AF leads to the appearance of very frequent, low-amplitude and irregular waves f. The amplitude of these waves varies in different patients and in different ECG leads: in some leads, the f waves may be imperceptible, whereas in other leads (especially in lead V1) they can be so pronounced that it is possible to assume the presence of TP, although atrial activity has more high frequency, than it usually happens when trembling. Teeth P, of course, absent.

2) Atrioventricular conduction during atrial fibrillation. Fortunately, the AV-node is not able to conduct all the atrial impulses on the ventricles: if this were possible, the VF would develop as a result! Some impulses are completely blocked, others only partially penetrate the AV node and therefore do not excite the ventricles, but can block or delay the passage of subsequent impulses. This process of “latent holding” is responsible for the irregular rhythm of the ventricles, which is the hallmark of this arrhythmia.

The absence of P-waves (even in the absence of noticeable f waves) and an irregular ventricular rhythm indicate the presence of AF. AF with a high frequency of ventricular contractions is often not diagnosed. Errors can be avoided by remembering that an irregularity of ventricular rhythm is a characteristic feature of arrhythmia. However, if against the background of AF, complete AV block develops, then the ventricular rhythm, of course, becomes slow and regular. The frequency of ventricular contractions in AF depends on the conductive ability of the AV node, which, in turn, is affected by the autonomic nervous system.

ECG in atrial fibrillation (AF)

ECG in atrial fibrillation (AF)

Atrial fibrillation (AF) is characterized by an absolutely irregular ventricular rhythm and the absence of teeth R. It can be paroxysmal, persistent or permanent (in the Russian-language literature in relation to permanent AF, the terms “permanent” or “chronic” are often used). Causes may include hypertension, MI, cardiomyopathy, valvular heart disease, hyperthyroidism, SSS, and alcohol use. Often, arrhythmia is idiopathic. Its prevalence increases with age, the probability of its occurrence throughout life is 26%.

An individual approach to treatment is necessary, taking into account the etiological factors, clinical manifestations and risks of the arrhythmia itself. Although in most cases it is possible to restore sinus rhythm using cardioversion, quite often the arrhythmia recurs. You can stop and / or prevent the recurrence of OP using flekainid, amio-daron and sotalol, but not digoxin. The frequency of ventricular contractions in AF can be controlled using calcium channel blockers or BAB; use of digoxin may not be enough to control the rhythm, especially during physical exertion.

Stratification of the risk of systemic emboli using the CHA2DS2VASc scale allows you to choose how to prevent these complications with non-valvular AF: taking aspirin, indirect anticoagulants (for example, warfarin or dabigatran) or performing an intervention to occlude the left atrium (LP) using a special device.

Atrial fibrillation in mitral stenosis.

Atrial fibrillation in mitral stenosis.

Atrial fibrillation in itself is not life threatening. The prognosis is usually relatively favorable, even considering the risk of arterial thromboembolism. About 10% of patients develop heart failure. Mortality of patients with atrial fibrillation is 1.5-1.9 times higher than mortality in the population as a whole.

For the treatment of patients with atrial fibrillation, it is recommended to first translate the tachyarrhythmic form of blink into normal arrhythmic with the help of drugs (for example, cardiac glycosides, verapamil, beta-adrenergic receptor blockers) and at the same time to prescribe anticoagulant therapy. Then it is necessary to clarify the cause of atrial fibrillation and, depending on this cause (for example, valve defect or hyperthyroidism), to perform a surgical intervention or to select a medical therapy.

In the absence of a reason that can be directly affected, the patient’s data should be discussed in order to present what the prospects for drug or electrical cardioversion are and how appropriate they are. This primarily depends on how long the atrial fibrillation lasts (for example, less than 6 months or more than this period), how much the LP is increased (for example, does its diameter exceed 50 mm or is it less than 50 mm) and does flicker manifest Atrial clinical symptoms.

If you intend to perform cardioversion, then for 3 weeks. before the proposed date of this treatment procedure, the patient is prescribed anticoagulants and, only after achieving effective hypocoagulation, they proceed to medication (using flecainide, etacizin, propafenone, beta-adrenergic receptor blockers, cardiac glycosides, amiodarone, and new drugs of dronedarone or vernacalanta) or an electric cardiac glycoside, amiodarone, and new drugs of dronedarone or vernacalanta or an electric cardonic glucoside, amiodarone, and new dronedarone or vernacalanta treatment. Additionally prescribe drugs that stabilize the rhythm of heart contractions.

Patients whose rhythm disturbance is asymptomatic, elderly patients, as well as those for whom, based on the above criteria, cardioversion seems to have little promise, after long-term anticoagulant therapy should be treated only with heart rhythm-stabilizing drugs, in particular beta-adrenergic receptor blockers or cardiac glycosides.

Patients with clinical manifestations of atrial fibrillation, resistant to drug or electrical cardioversion, can be X-ray-surgical isolation of the orifices of the pulmonary veins by radiofrequency ablation or cryodestruction. Successful results after such interventions are observed in 70% of patients.

The auricle of the left atrium (LP) is the most frequent site of the formation of blood clots, which become the source of thromboembolism. Recently, a new method of treatment has been developed, which made it possible to reduce the risk of thromboembolism in patients with atrial fibrillation, which can be used especially in cases where the administration of anticoagulant therapy is contraindicated. With this method of treatment, which is abbreviated as PLAATO, the ear of the brain is isolated from its cavity by implanting an umbrella-like device into the atrium using catheter technology.

Flicker examples

The following 3 forms of atrial fibrillation are distinguished:

• paroxysmal: duration not more than 2 days, spontaneous cessation of an attack;
• persistent: duration exceeds 7 days, arrhythmia can be eliminated;
• permanent: lasting more than one year, usually not stopped.

Atrial fibrillation associated with vagotonia usually appears at night or at rest, while with sympathicotonia, atrial fibrillation appears as a result of physical or psycho-emotional stress.

Atrial fibrillation is usually caused by an organic lesion of the heart, for example, ischemic heart disease, hypertension, mitral stenosis or mitral insufficiency, dilated or hypertrophic cardiomyopathy. There are also cases of idiopathic atrial fibrillation (atrial fibrillation, in 15% of cases). Patients with atrial fibrillation often complain of palpitations, a feeling of lack of air, interruptions in the work of the heart, and general weakness.

From a pathophysiological point of view, the occurrence of atrial fibrillation can be explained as follows. Flicker usually occurs in the PL, in particular due to the focal trigger activity of the atrium wall near the mouths of the pulmonary veins. Multiple paths of re-entry of excitation waves lead to arrhythmias, electrical tissue restructuring and structural changes. As a result, the atria lose their ability to contract and expand.

Blood stasis in the enlarged and non-contractile left atrium (LP) increases the risk of thromboembolism by 5-7 times compared with the risk of this complication in the population. Thromboembolism occurs in 20% of patients with atrial fibrillation, and in 80% of cases thromboembolism of cerebral arteries is observed. To reduce the risk of this complication, patients with atrial fibrillation are prescribed anticoagulants.

Signs of atrial fibrillation on ECG

Signs of atrial fibrillation on ECG

Normal P teeth are not identified, fibrillation waves are seen, having different configurations.

Due to the chaotic conduct of excitation from the atria to the ventricles, a picture of absolute arrhythmia is noted.

Atrial fibrillation is the most frequent heart rhythm disorder requiring treatment. It usually appears in IHD, AH, mitral heart disease and hyperthyroidism.

The treatment is carried out with anticoagulants and antiarrhythmic drugs, electrical cardioversion, and only in the absence of the effect of these funds is shown catheter ablation of the pathways in the mouth of the pulmonary veins.

Atrial fibrillation is the most frequent heart rhythm disorder requiring treatment. In recent years, new data on the pathogenesis of atrial fibrillation have been accumulated, new methods of diagnosing and especially treating this disease have been developed.

Atrial fibrillation is observed in 1% of the adult population. In Germany, patients with atrial fibrillation are 1 million. With increasing age, especially after 80 years, the frequency of atrial fibrillation increases, reaching 10-16%.

When atrial fibrillation occurs, the occurrence of arousal is completely disturbed, the sinus rhythm disappears, and the normal R-wave stops registering on the ECG. Instead, so-called flicker waves (f) are registered, randomly following each other. Flicker waves are very small and sometimes inexperienced remain unnoticed. The frequency of flicker waves is 350-600 per minute. They are characterized by inconstancy of shape and size, and sometimes they are not even separated from each other.

Atrial fibrillation waves are conducted to the ventricles without any pattern, so the RR interval is irregular, which suggests an absolute arrhythmia. Usually the waves f are most clearly visible in leads II and / or V). The QRS complex, as a rule, is not wide, there are no pathological changes in the ST interval at first.

If the frequency of ventricular contractions in atrial fibrillation does not exceed 60 per minute, they speak of bradyarrhythmic flicker, but if it is more than 100 beats per minute, then it is tachyarrhythmic. In these cases, treatment is necessary.